One of the most important diseases limiting tomato production in tropical areas is bacterial wilt, caused by the soil-borne bacterium, Pseudo-monas solanacearum E. F. S. Breeding for resistance has proved to be the best way to control bacterial wilt in several crops. Similarly, it appears that successful commercial production of tomato in many parts of the tropics requires the development of tomato varieties resistant to the pathogen. A voluminous literature, approaching 1,000 papers has been published on the subject of bacterial wilt. The genetics of resistance to the disease, however, has been investigated in only a few crops. Resistance is governed by multiple genetic factors in tobacco (Smith and Clayton, 1948) and is suspected to be similarly multifactorial in other species (Singh, 1961). Many attempts have been made to control bacterial wilt by chemical and physical treatments of soil (Stevens, 1906, Garner et al., 1917; Smith:, 1944; 1947; and Sequeira, 1958). With few exceptions, however, chemical means of reducing losses due to wilt have not been practical (Kelman, 1953) because of phytotoxicity or expense of application. Tomato breeders have been unsuccessful in producing commercial varieties immune to bacterial wilt. A useful source of genetic resistance, however, is available in Lycopersicon pimpinellifolium Mill. The present study was based on this resistant source material. The major objectives of the investigation were: to investigate the inheritance of resistance to bacterial wilt in tomato, to estimate the degree of environmental modification of resistance, and to determine whether resistance is linked with the sp+ (indeterminate growth) and Mi+ (nematode susceptibility) loci on chromosome 6.

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Theses for the degree of Doctor of Philosophy (University of Hawaii (Honolulu)). Horticulture; no. 37

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